Hyperoside inhibits Mitochondrial DNA Damage to Reverse Hepatocyte Pyroptosis to Treat Doxorubicin-related Hepatotoxicity

ABSTRACT

Background: Hyperoside is a potential liver cell and mitochondrial protector, but there is no evidence to suggest that hyperoside can effectively treat doxorubicin (DOX) related liver toxicity. Objectives: This study aims to determine the role of hyperoside in DOX related liver toxicity and liver cell damage in vivo and in vitro. Materials and Methods: A mouse model of liver toxicity was induced by intraperitoneal injection of DOX, and hyperoside was administered orally for treatment. During this period, the weight and food intake of the mice were recorded. The morphology of mouse liver tissue was observed by hematoxylin and eosin staining. Oxidative stress and inflammatory status in mice were observed through serum inflammatory factors and liver oxidative stress markers. Mitochondrial damage is determined by the degree of mitochondrial DNA damage. Western blotting and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the expression of pyroptosis and genes in the liver and liver cells. Results: Hyperoside can effectively treat DOX-induced oxidative stress and inflammatory status, liver function damage, and hepatocyte necrosis in mice. Further research suggests that the beneficial effect of hyperoside is achieved by inhibiting mitochondrial DNA damage in liver cells. Conclusion: This study indicates that hyperoside improves DOX-induced liver toxicity by inhibiting mitochondrial DNA damage.

KEYWORDS

• Hyperoside
• doxorubicin
• hepatotoxicity
• pyroptosis
• mitochondria

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• DOI10.1177/09731296241306199Copy

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